Drug for treating vasculogenesis mediated diseases and application

Abstract

The invention belongs to the technical field of medicine, discloses a drug for treating vasculogenesis mediated diseases and application and provides the drug for treating the vasculogenesis mediateddiseases prepared by using arsenic trioxide. A method for evaluating a treatment effect of the drug for treating the vasculogenesis mediated diseases comprises the steps: evaluating an inhibiting effect on a blood vessel multiplication functional module of arthropathy synoviocyte TSP-1-TGF-beta-CTGF-VEGF caused by arsenic trioxide; evaluating an inhibiting effect on multiplication of capillary endotheliocyte of pathological joints caused by arsenic trioxide through inhibiting the blood vessel multiplication functional module of the TSP-1-TGF-beta-CTGF-VEGF. According to the drug and the application, the arsenic trioxide can be used for inhibiting blood vessel multiplication through inhibiting the functional module of the TSP-1-TGF-beta-CTGF-VEGF, thereby playing a role in treating blood vessel multiplication diseases.

Description

technical field [0001] The invention belongs to the technical field of medicine, and in particular relates to a medicine for treating angiogenesis-mediated diseases and its application. Background technique [0002] Blood vessels form an extensive network throughout the body, supplying oxygen and nutrients to every part of the body, and abnormal blood vessel growth and function are hallmarks of cancer as well as inflammatory diseases, leading to disease progression. Local lesions in vascular proliferation-related joint diseases rely on neovascularization to ensure a continuous supply of oxygen and nutrients to diseased and inflammatory cells. Under physiological conditions, the synovial lining of the joint is only composed of 1-2 layers of cells. In pathological conditions of arthropathy such as RA, inflammatory cytokines such as TNF-α and IL-1 promote a significant increase in the number of synoviocytes, usually reaching 4-10 layers. The fibroblast-like synoviocytes (FLS)...

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Problems solved by technology

Vascular proliferation is one of the early histopathological changes in rheumatoid arthritis (RA), and it is a necessary condition for pannus formation, but its mechanism is still unclear; current analysis shows that thrombospondin-1 (TSP-1), transformed growth Factor-β1 (TGF-β1), connective tissue growth factor (CTGF), and vascular endothelial growth factor (VEGF), these angiogenic factors have increased expression in the synovial tissue of RA patients and may interact with each other to promote vascular proliferation in RA synovial tissue. have an important impact

Although biologics anti-TNF-α therapy is effective for RA, it is worrying that this treatment will cause a variety of adverse reactions, and even increase the incidence of malignant tumors; arsenic trioxide (As 2 o 3 ) has been used to treat vascular proliferative diseases such as tumors, which has attracted widespread attention worldwide; however, As 2 o 3 The role and molecular mechanism of synovial angiogenesis in RA patients are still unclear

[0014] In the treatment of arsenic trioxide, the specific binding protein or target that exerts the anti-angioproliferative effect by inhibiting the TSP-1-TGF-β-CTGF-VEGF functional module is still unclear and needs to be further studied; the difficulty lies in the fact that the human body is a complex There are tens of thousands of protein molecules in the system. Therefore, to find the specific target protein molecules of arsenic trioxide requires further investment of time and energy; Unclear, pending further study

[0015] In summary, the problem in the prior art is that TNF-α antagonists also have their limitations

TNF-α antagonists can cause latent tuberculosis infection or lead to latent tuberculosis relapse

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